The cardiovascular response to 25% of blood volume loss.

A 25% blood loss is a grade 2 classification of shock and non- progressive stage(sometimes called the
compensated stage) - normal circulatory compensatory mechanisms eventually cause full recovery
without help from outside therapy.

When a person rapidly loses 25% of total blood volume from a large vein, the inadequate intravascular
volume causes sequential decreases in central blood volume, venous return, ventricular filling, stroke
volume, cardiac output, and thus mean arterial pressure. However, if the blood loss comes from a large
peripheral artery, the mean arterial pressure in central arteries does not fall until cardiac output falls
secondary to decreased venous return. Of course, if the blood loss occurs from a blown aortic aneurysm,
mean arterial pressure falls immediately.

After its abrupt initial fall, arterial pressure tends to return to normal, although blood pressure falls
irreversibly in some cases. Under favorable circumstances, the body restores blood pressure toward
normal values by mobilizing two lines of defense. First, circulatory control mechanisms act on the heart
and blood vessels to restore cardiac output and to increase peripheral resistance. Second, mechanisms
of capillary exchange and fluid conservation restore the intravascular volume.

After hemorrhage, cardiovascular reflexes restore mean arterial pressure

Several cardiovascular reflexes cooperate to compensate for the fall in mean arterial pressure. These
reflexes originate from four major groups of receptors.

1. High-pressure baroreceptors. The fall in arterial pressure leads to a decrease in the firing rate of
afferents from the carotid and aortic baroreceptors. The resulting enhanced sympathetic output and
diminished vagal output increase heart rate and cardiac contractility and also produce venoconstriction
and selective arteriolar constriction. These responses cooperate to re-establish the arterial pressure.

2. Low-pressure baroreceptors. Reduced blood volume directly decreases effective circulating volume,
which in turn lessens the activity of low-pressure stretch receptors. The resulting increased sympathetic
outflow causes vasoconstriction in a number of vascular beds, particularly the kidney, reducing
glomerular filtration rate and urine output. In response to decreased stretch, low-pressure receptors at
various sites in the circulation ultimately have divergent effects on heart rate. The atrial stretch
receptors also instruct the hypothalamus to enhance release of AVP, which reduces renal water
excretion. During shock, the vasoconstrictor effects of AVP appear to be important for maintaining
peripheral vascular resistance. Reduced atrial stretch also lowers the level of circulating atrial natriuretic
peptide (ANP) thereby reducing salt and water loss by the kidneys.

3. Peripheral chemoreceptors. As blood pressure drops, perfusion of the carotid and aortic bodies
declines, causing local hypoxia near the glomus cells and an increase in the firing rate of the
chemoreceptor afferents, a response enhanced by increased sympathetic tone to the peripheral
chemoreceptor vessels. Increased chemoreceptor discharge leads to increased firing of the sympathetic
vasoconstrictor fibers and ventilatory changes that indirectly increase heart rate.

4. Central chemoreceptors. Hypotension results in brain ischemia, which leads to a fall in the image of
brain ECF as well as a rise in image and a fall in pH. The acidosis has a profound effect on the central
chemoreceptors in the medulla. leading to a sympathetic output several-fold more powerful than that
caused by baroreceptor reflexes.

These four reflex pathways have in common the activation of a massive sympathetic response that
results in the release of norepinephrine from postganglionic sympathetic neurons. In addition, the
sympathetic response triggers the adrenal medulla to release epinephrine and norepinephrine roughly
in proportion to the severity of the hemorrhage. Lowering of the mean arterial pressure to 40 mm Hg
causes circulating levels of epinephrine to rise 50-fold and those of norepinephrine, 10-fold. The
consequences of the four combined reflex actions are the following response:

Tachycardia and Increased Contractility.

Increased sympathetic activity increases heart rate roughly in proportion to the volume of shed blood.
Thus, the degree of tachycardia is an index of the severity of the hemorrhage. Increased sympathetic
tone increases myocardial contractility but can increase stroke volume only after venous return also
improves.

Arteriolar Constriction.

Sympathetic constriction of the resistance vessels is most pronounced in the blood vessels of the
extremities, skin, skeletal muscle, and abdominal viscera. Although both precapillary and postcapillary
resistance vessels constrict, the precapillary response initially dominates. As a result, capillary pressure
falls precipitously, leading to the transcapillary refill discussed in the next section. Renal blood flow falls
rapidly after hemorrhage as a result of the fall in blood pressure but recovers after a few minutes
because of autoregulation. The responses of both high- and low-pressure stretch receptors lead to
enhanced sympathetic vasoconstrictor traffic to the kidney. Although renal blood flow has a high
threshold for this sympathetic traffic, the sympathetic vasoconstriction eventually overrides renal
autoregulation if arterial pressure remains low or continues to fall. In hypovolemic shock, renal blood
flow falls to a proportionately greater extent than does cardiac output, which explains why severe
hemorrhage often results in acute renal failure. Blood flow in the medulla of the kidney is less
compromised than in the cortex, leading to “medullary washout” of the hypertonic interstitial fluid in
the renal medulla and an inability to produce a concentrated urine. Both coronary blood flow and
cerebral blood flow initially fall after hemorrhage, but autoregulation can largely restore blood flow to
normal.

Venous Constriction.

The fall in blood volume with hemorrhage occurs primarily in the large-capacitance vessels, especially
those that contain the central blood volume. These vessels are very sensitive to sympathetic stimulation
(which causes constriction) and less so to local metabolites (which causes dilation). The sympathetic
venous constriction decreases both the capacity and the compliance of the large veins, thereby tending
to restore central venous pressure. In addition, sympathetic venous constriction increases postcapillary
resistance, which is important for transcapillary refill.
Circulating Vasoactive Agonists

As already discussed, sympathetic stimulation of the adrenal medulla causes circulating epinephrine
levels to rise. In addition, sympathetic stimulation of the granular cells in the juxtaglomerular apparatus
of the kidney leads to an increased release of renin and, ultimately, increased plasma levels of
angiotensin II (ANG II). In hemorrhagic shock, ANG II rises to concentrations that are vasoconstrictive.
Activation of the sympathetic system also triggers sympathetic cholinergic stimulation of the sweat
glands, causing the patient's extremities to become clammy.

With moderate blood losses (15% to 30%), these four responses can increase total peripheral resistance
sufficiently to keep arterial pressure at about normal levels. However, cardiac output remains
depressed.

What is the cardiovascular response to 25% of blood volume loss?

CARDIOVASCULAR RESPONSE TO 25% OF BLOOD VOLUME LOSS

Blood volume loss can lead to hemorrhagic shock. So, by using blood volume loss, we can classify
hemorrhagic shock. According to Hooper &. Armstrong(2021), the The American College of Surgeons
Advanced Trauma Life Support (ATLS), classifies hemorrhagic into 4 classes;

1. Class I – Volume loss up to 15%

2. Class II – Volume loss of 15-30%

3. Class III – Volume loss of 30-40%

4. Class IV – Volume loss over 40%

Each class has its own consequences, some of which may overlap, but for this question we will
concentrate on the effects of 25% volume loss.

A 25% blood volume loss is class II classification of hemorrhagic shock (Hooper & Armstrong, 2021). An
average person of 70kg has a blood volume loss of 15-30%, approximately 750 to 1500ml, when using a
total blood volume of 5000ml (Hooper & Armstrong, 2021).

When this type of volume loss occurs,

1. Pulse pressure decreases

2. Heart rate increases (100-120/min)

3. Respiratory rate increases (20-30/min)

4. Urine output reduces (20-30ml/hr)

5. The patient is mildly anxious

6. Blood pressure remains normal.

The volume loss results in autonomic and neurohormonal effects. In this case, since we are discussing
cardiovascular response, we shall concentrate on the autonomic effects.

The baroreceptors rapidly respond to the rate of rise or fall in arterial pressure and therefore adjusts the
pulse pressure accordingly. This is because the baroreceptor reflex is extremely sensitive to changes in
mean arterial pressure (Rhoades & Bell, 2013).

The neurohormonal effects of blood volume loss is by the RAAS (Renin- Angiotensin-Aldosterone
System). When the baroreceptors activate the sympathetic system, they act on the beta-2 receptors
activating the RAAS cascade to reabsorb water and salt (Rhoades & Bell, 2013). Increasing vascular
resistance and blood volume which ultimately increases blood pressure.

In the autonomic system, the baroreceptors are responsible for the cardiac response to volume loss.
With hypovolemia, the volume loss activates the sympathetic system which activates two types of
receptors. The alpa-1 adrenergic receptors and the beta-1 receptors.

The alpha-1 receptors are found on the blood vessels in larger numbers than beta-2 adrenergic
receptors (Rhoades & Bell, 2013). Their activation through the sympathetic system will cause
vasoconstriction and an increase in systemic vascular resistance (Rhoades & Bell, 2013).

The beta-1 adrenergic receptors are found in the sinoatrial node, atrioventricular node, specialized
conducting tissue of the heart and the cardiac muscle. Their activation through the sympathetic system
will cause an increase in heart rate, contractility and conduction velocity (Rhoades & Bell, 2013).

The changes in baroreceptor stretch, due to arterial pressure, causes reflex activation of the
cardiovascular system, by changes in the baroreceptor firing rate and therefore activating the
sympathetic or parasympathetic activity.
A 15-30% volume loss will cause arterial hypotension and a decreased cardiac output. The arterial
hypotension causes a baroreceptor stretch to be reduced. This increases the sympathetic neural activity
and decreases the parasympathetic activity to result in increased stroke volume, heart rate and systemic
vascular resistance in attempt to return the blood pressure back to normal (Rhoades & Bell, 2013). The
sympathetic activity in turn activates the beta-1 adrenergic receptors which force contraction of the
heart (therefore increasing stroke volume) and increase heart rate(Rhoades & Bell, 2013). This in turn
increases cardiac output to increase arterial blood pressure.

The sympathetic activity also activates the alpha-1 adrenergic receptors to increase systemic vascular
resistance, which also increases arterial pressure(Rhoades & Bell, 2013). This decrease in venous
compliance shifts volume centrally, increasing right atrial pressure and thereby stroke volume.

In conclusion, the cardiovascular system will respond to class II hemorrhagic shock by increasing the
arterial pressure, using the sympathetic system, in an attempt to maintain the arterial pressure.

REFERENCES
Hooper N, Armstrong TJ. (2021), Hemorrhagic Shock. [Updated 2021 Jul 13]. In: StatPearls [Internet].
Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK470382/

Rhoades, RA. Bell DR. (2013) Medical physiology: Principles for clinical medicine, 4th Ed. Lippincott
Williams & Wilkins